New insights into the impact of injury on cartilage cells

Documented in extensive studies, backed by the anecdotal evidence of professional athletes, impact injury to joints causes degeneration of cartilage. In most cases, the eventual result is the pain, stiffness, and compromised mobility of osteoarthritis (OA). Yet, questions remain surrounding the role of the inflammatory system in the cartilage destruction following mechanical trauma.

Tissue damage typically stimulates an influx of leukocytes, white blood cells known for promoting tissue regeneration and healing--to tissue protecting organs. However leukocytes can be a double edged sword. In the May 2006 issue of Arthritis & Rheumatism (http://www.interscience.wiley.com/journal/arthritis), researchers at Baylor College of Medicine and the Michael E DeBakey Veterans Affairs Medical Center in Houston, Texas, present the results of a study to test the hypothesis that leukocytes extend the zone of damage and cell death in cartilage after an acute injury.

The research team began with a collection of dog bones--the hind knee joints of 24 fresh young adult cadaver canines. Within one hour after death, each bone was subjected to impact injury with a metal weight, determined sufficient to cause cartilage damage without shattering the bone. A comparable collection of cadaver canine bones was preserved to serve as controls. All of the knee joints were cultured with blood leukocytes from the same dogCartilage biopsies were taken at various intervals between 12 hours and 7 days.

Among the assaulted bones, approximately half of the chondrocytes, or cartilage cells, died within 7 days. In the uninjured bones, over 90 percent of the chondrocytes survived. A surprising finding was the reduced viability of cartilage cells located well outside the vicinity of direct impact.

Contact: Amy Molnar
John Wiley & Sons, Inc.

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